Recurrent hemichorea following a single infarction in the contralateral subthalamic nucleus (original) (raw)
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Hemichorea–hemiballism syndrome following a thrombo-embolic striatal infarction
Neurological Sciences, 2013
A 70-year-old man was admitted to our emergency department for sudden onset of abnormal involuntary movements involving his upper and lower left limbs. Hemichoreal movements were restricted to his left limbs, associated with rare episodes of hemiballism (video). There were no cranial nerve alterations, no sensory loss or limb weakness. The patient reported mild hypertension under treatment. There was no history of diabetes mellitus or epilepsy, no prior exposure to neuroleptics or recent change in therapy. He denied any similar previous episode or family history of movement disorders. Chest radiography, electrocardiography, and laboratory tests including glucose, glycated hemoglobin, coagulation parameters, and immunoglobulin electrophoresis were normal. Brain non-contrast CT scan on admission showed no signs of acute ischemia (Fig. 1a). A supra-aortic-trunk Doppler sonography revealed an irregular surface plaque, partly ulcerated, on the origin of the right internal carotid artery with stenosis of about 90 %, confirmed at CT angiography (Fig. 1b).
Pituitary apoplexy associated with acute cerebral infarct
Journal of Clinical Neuroscience, 2008
Chorea/ballism is the commonest movement disorder following stroke, particularly in elderly patients. 2,4 Patients with deep hemorrhagic lesions have a higher probability of developing movement disorders. 2 In previous reports of vascular hemiballism, ischemic lesions were responsible for the majority of cases, whereas hemorrhagic lesions were responsible for less than 20% of cases. 1-8 The latter were massive thalamic hemorrhages in many cases. 2,8 Small isolated hemorrhagic STN lesions have been reported only in the series by Chung et al. 3 They presented three such cases and suggested a relatively high frequency of hemorrhagic lesions in the STN. No case of hemorrhagic infarct, as found in our case 2, has been reported previously. The outcome of hemiballism is usually benign. 1-5,7,8 Stroke is the most common underlying cause in patients who experience spontaneous improvement. 4 However, vascular hemiballism caused by STN lesions tends to be more severe than that caused by lesions elsewhere. 1 Chung et al. 3 reported that the rate of spontaneous resolution was significantly higher in patients with cortical strokes than in those with STN lesions. Hemiballism persisted in their three patients with hemorrhagic STN lesions. This might be due to the actual destruction of the basal ganglia-thalamocortical circuitry. In contrast, the present two patients showed rapid and complete recovery. Although accompanied by perifocal edema, the lesions (i.e., a T 1 high-intensity lesion in case 1 and a high-intensity lesion on diffusion-weighted imaging in case 2) were small in size and were confined to the STN. In addition to perifocal edema of the hemorrhage or infarction, the partial destruction and plastic responses of the STN may explain in transient hemiballism. Furthermore, compensation by various connecting circuits may have participated in our patients' excellent recovery since the STN is significantly more interconnected than originally believed. 1 The prognosis for patients with hemiballism caused by a large lesion involving the STN is usually poor, probably because not only the STN, but also its afferent and efferent pathways, are affected. Thus, precise evaluation of the affected region with MRI is useful in predicting the prognosis.
Journal of Stroke and Cerebrovascular Diseases, 2020
Hemichorea and other hyperkinetic movement disorders are a rare presentation of stroke, usually secondary to deep infarctions affecting the basal ganglia and the thalamus. Chorea can also result from lesions limited to the cortex, as shown in recent reports. Still, the pathophysiology of this form of cortical stroke-related chorea remains unknown. We report 4 cases of acute ischemic cortical strokes presenting as hemichorea, with the infarction being limited to the parietal and insular cortex in perfusion computed tomography scans and magnetic resonance imaging. These cases suggest potential dysfunction of pathways connecting these cortical regions with the basal ganglia.
Stroke, 1986
Lacunar infarcts in the basal ganglia are known to cause various movement disorders, such as chorea, focal dystonia, and hemlchorea-hemiballlsmus. We report here a case of putaminal lacunar infarction which presented with "painful tonic spasms" of the contralateral limbs. This consisted of paroxysmal brief, painful, flexor contractures of the upper, and occasionally the lower limb. These were not focal seizures but were controlled with carbamazepine, which has been used for the "painful tonic spasms" wellassociated with multiple sclerosis. The putaminal infarct we describe is probably related to a lupus anticoagulant and systemic lupus erythematosus.
Hemichorea-Hemiballism in A 50-Year-Old Man With Newly Diagnosed Diabetes
AACE Clinical Case Reports, 2021
Objective: Hyperglycemia may cause acute central nervous system dysfunction manifesting as agonizing involuntary movements due to insult to the basal ganglia. We report a case of hemichorea-hemiballism (HCHB) in a patient with diabetes. Method: Clinical assessment of the patient was performed, along with laboratory tests and brain imaging. Results: The patient was a 50-year-old man with newly detected diabetes with persistent involuntary movement of the right upper and lower limbs for few weeks. The involuntary movement was nonrhythmic, nonpatterned, purposeless, and often jerky with variable amplitude and frequency, sometimes wild and flailing in the form of hemichorea with a ballistic component (HCHB). He had a history of poor compliance to prescribed oral antidiabetic drugs. At presentation, although he was hemodynamically stable, random capillary blood glucose level was 18 mmol/L and glycated hemoglobin A1 level was 15.1% (141.5 mmol/mol). Clinical examination did not reveal any focal deficit or positive Babinski sign. There was a hyperintensity in the left basal ganglia region in T1-weighted magnetic resonance imaging (MRI) of the brain, which was iso-to-hyperintense in T2-weighted image and fluid-attenuated inversion recovery sequence. There was no restriction of diffusion on the diffusion-weighted image or blooming on gradient echo sequences, indicating absence of infarction or hemorrhage. Control of hyperglycemia resulted in disappearance of the involuntary movement within 1 month. Conclusion: While there are many differential diagnoses for HCHB, the clinical scenario suggests hyperglycemia as the underlying cause in this patient. This case reiterates that multiple central nervous system manifestations may be attributable to diabetes.